Infection is currently regarded as one of the major causes of dental implant failures. Recent clinical studies have shown that a characteristic, subgingival microflora can be isolated from implants 1-3 weeks following placement. Importantly, key bacteria found in these early microbial communities have also been strongly associated with tissue destruction and bone loss in Localized Juvenile Periodontitis (LJP) and Adult Periodontitis. Therefore, it is conceivable that early colonization by these specific microorganisms may preclude host tissue integration and lead to failure of the implant. Currently, little is known concerning how potential bacterial pathogens colonize implant surfaces. As a beginning to understanding these processes, we propose to: (1) delineate differences in the ability of representative healthy-implant site microorganisms and potential bacterial pathogens to adhere to Ti implant surfaces of differing surface roughness, and (2) determine if these representative microorganisms adhere to the different implant surfaces via non-interacting sites or through more complex interactions involving positive or negative cooperativity (defined as the changing probability of receptor-ligand interactions due to prior occupation of adjacent sites). It is our contention that the development of a reproducible, implant-bacterial adhesion model will aid significantly in our assessment of the physico- chemical nature of implant surfaces which promote host tissue integration while concurrently limiting bacterial colonization.